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Re: Neurobiology of functional recovery after stroke

Gainotti et al [1] find that the recovery over time of non-treated depressed patients with stroke was less than the non-depressed and the depressed but treated patients with stroke and was particularly manifested on the Rivermead mobility index. Neurobiological features are suggested by the correlation of the rate of speech hesitation pauses of 1 s (SHP), 4.79+/-2.48/min, 1.50+/-0.33 s (mean+/-SD), behavioral correlates of mood, with immobility in the face of stress, the state of the circulation (angina/hypertension) and sixfold incidence of clinical coronary heart disease (CHD) in two groups of men with normal coronary structure followed prospectively for 10 years, P<0.05 [2]. Depression independently and negatively influences autonomic control of heart rate in patients with acute myocardial infarction [3].

These findings are supported by: the correlation of rate and variability in duration of SHP with the left and right hemisphere, respectively; and an exaggerated cerebral cortical response and exaggerated asymmetry to mental stress in patients with CHD; profound effects on angina through consciously focusing attention on breathing and intervening pauses; the association of the reduction of blood pressure with longer, less recurrent SHP (about 2 s); and reports that the microvascular response to the onset of neural activity is delayed consistently about 3 s and is linked to increased coherence of electroencephalograph gamma-band activity (30-50 Hz or broader, centered on 40 Hz) associated with the execution of more complex tasks.

These findings give precise, objective methods with which to evaluate the effect of mental stress on the microvasculature and suggest interventions reduce the risk of vascular events, optimize mood, and enhance performance. Therefore, cognitive-behavioral and/or pharmacotherapeutic intervention to balance asymmetric brain functions and alleviate depression can be evaluated by the analysis of pauses on a time- base. This method is supported by reports that exaggerated heart rate oscillations during slow deep breathing in meditation is a dynamic state that increases effective connectivity between distinct cortical systems by the entrainment of gamma-frequency oscillations [1], counterbalancing the distributed anatomical and functional organization of brain activity, enabling the emergence of coherent behavior and cognition [4].

References (1) Gainotti G, Antonucci G, Marra C, Paolucci S. Relation between depression after stroke, antidepressant therapy, and functional recovery. J Neurol Neurosurg Psychiatry 2001;71:258-261.
(2) Friedman EH. Socioeconomic inequalities in cardiovascular disease (letter). Eur Heart J 2001;22:715.
(3) Pitzalis MD, Iacoviello M, Fioretti A, Guida P, Massari F, Mastropasqua F, Dello Russo G, Rizzon S. Depression but not anxiety influences the autonomic control of heart rate after myocardial infarction. American Heart Journal 2001;141:765-771.
(4) Varela F, Lachaux JP, Rodriguez E, Martinerie J. The brainweb: phase synchronization and large-scale integration. Nature Reviews Neuroscience 2001;2:229-239.

Ernest H. Friedman, MD